Tretazicar is a dinitrobenzamide prodrug that is converted in the presence of the enzyme NQO2 and co-substrate caricotamide (EP-0152R) into a potent cytotoxic bifunctional alkylating agent. Tretazicar is a product that belongs to a family of products used in the treatment of cancer because of its capacity to kill cells. The enzyme that activates tretazicar is present in leishmania cells where the product can be transformed and be active. Tretazicar kills infected cells by binding to the genetic material (DNA) of the cells and creating bonds that disrupt the genetic material and its function, finally resulting in the death of the infected cell. On 4 February 2008, orphan designation EU/3/08/529 was granted by the European Commission to Morvus Technology Limited, United Kingdom, for tretazicar for the treatment of visceral leishmaniasis. On 4 February 2008, orphan designation EU/3/08/529 was granted by the European Commission to Morvus Technology Limited, United Kingdom, for tretazicar for the treatment of visceral leishmaniasis. Tretazicar had been in phase II clinical trial for the treatment of liver cancer. However, this development was discontinued.

Rivenprost (ONO-4819) is a potent and selective EP4 receptor agonist. This compound can increase bone formation by stimulating osteoblast differentiation and function, possibly by modulating mesenchymal cell differentiation. Rivenprost has also been studied for its potential to prevent bone loss (in osteoporosis) and stabilize bone implants. Combined with risedronate, rivenprost may be an effective treatment for osteoporosis. A phase II study evaluating rivenprost in ulcerative colitis was terminated in 2009.

Tosedostat is a proprietary orally bioavailable inhibitor of the M1 family of aminopeptidases with potential antineoplastic activity. Tosedostat is converted intracellularly into a poorly membrane-permeable active metabolite (CHR-79888) which inhibits the M1 family of aminopeptidases, particularly puromycin-sensitive aminopeptidase (PuSA), and leukotriene A4 (LTA4) hydrolase; inhibition of these aminopeptidases in tumor cells may result in amino acid deprivation, inhibition of protein synthesis due to a decrease in the intracellular free amino acid pool, an increase in the level of the proapoptotic protein Noxa, and cell death. There are several ongoing Phase 2 cooperative group-sponsored trials and investigator-sponsored trials evaluating the clinical activity of Tosedostat in combination with standard agents in patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).